Evidence map›Paper›PMID 30207029›Full record

ArticleCancer science2018

PHLDA1, another PHLDA family protein that inhibits Akt.

Yu Chen, Masahiro Takikawa, Shuichi Tsutsumi, Yoko Yamaguchi, Atsushi Okabe, Mayuna Shimada, Tatsuya Kawase, Akane Sada, Issei Ezawa, Yuhei Takano and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.1field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. PHLDA2 in cancer: From molecular mechanisms to therapeutic opportunities.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Silencing of theFrontiers in pharmacology · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Yu ChenLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Masahiro TakikawaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Shuichi TsutsumiGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Yoko YamaguchiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Atsushi OkabeGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Mayuna ShimadaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Tatsuya KawaseLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Akane SadaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Issei EzawaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Yuhei TakanoLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Kisaburo NagataFaculty of Science, Department of Biomolecular Science, Toho University, Chiba, Japan.
Yutaka SuzukiLaboratory of Systems Genomics, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
Kentaro SembaDepartment of Life Science and Medical Bioscience, Graduate School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Rieko OhkiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID http://orcid.org/0000-0002-7775-6653
Waseda University · JPThe University of Tokyo · JPToho University · JPChiba University · JP

Funding

Applied Research for Innovative Treatment of Cancer from the Ministry of Health, Labour and WelfareDevelopment of Innovative Research on Cancer Therapeutics P-DIRECT/Ministry of Education, Culture, Sports, Science and Technology of JapanFoundation for Promotion of Cancer Research in JapanLife Science Foundation of JapanMitsubishi FoundationNational Cancer Center Research and Development FundNOVARTIS Foundation (Japan) for the Promotion of ScienceOkinaka Memorial Institute for Medical ResearchPrincess Takamatsu Cancer ResearchProject Mirai Cancer ResearchResearch for Innovative Treatment of Cancer from the Ministry of Health, Labour and WelfareThe Ministry of Education, Culture, Sports, Science and Technology of Japan #15K19537The Ministry of Education, Culture, Sports, Science and Technology of Japan #17H03587The Ministry of Education, Culture, Sports, Science and Technology of Japan #17H07378
6 · The paper itself

Abstract

The PHLDA family (pleckstrin homology-like domain family) of genes consists of 3 members: PHLDA1, 2, and 3. Both PHLDA3 and PHLDA2 are phosphatidylinositol (PIP) binding proteins and function as repressors of Akt. They have tumor suppressive functions, mainly through Akt inhibition. Several reports suggest that PHLDA1 also has a tumor suppressive function; however, the precise molecular functions of PHLDA1 remain to be elucidated. Through a comprehensive screen for p53 target genes, we identified PHLDA1 as a novel p53 target, and we show that PHLDA1 has the ability to repress Akt in a manner similar to that of PHLDA3 and PHLDA2. PHLDA1 has a so-called split PH domain in which the PH domain is divided into an N-terminal (β sheets 1-3) and a C-terminal (β sheets 4-7 and an α-helix) portions. We show that the PH domain of PHLDA1 is responsible for its localization to the plasma membrane and binding to phosphatidylinositol. We also show that the function of the PH domain is essential for Akt repression. In addition, PHLDA1 expression analysis suggests that PHLDA1 has a tumor suppressive function in breast and ovarian cancers.

Indexed as

Alternative SplicingAnimalsBreast NeoplasmsCell Line, TumorCell MembraneFemaleGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHeLa CellsHumansNeoplasm TransplantationOvarian NeoplasmsPhosphatidylinositolsProtein BindingProto-Oncogene Proteins c-aktPHLDA1 protein, humanPhosphatidylinositolsProto-Oncogene Proteins c-aktTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53Aktp53PH domainPHLDA familytumor suppressor

Identifiers

PMID30207029
PMCPMC6215895
OpenAlexW2889689714

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.